Hyperoxic Condition Promotes an Inflammatory Response during Cardiopulmonary Bypass in a Rat Model

Systemic inflammatory responses in patients receiving cardiac surgery
supported by cardiopulmonary bypass (CPB) significantly contribute to
CPB-associated morbidity and mortality. We hypothesized that hyperoxia
insufflation aggravates the inflammatory responses and organ damage
during CPB. To verify this hypothesis, we investigated the inflammatory
responses at high and normal levels of arterial pressure of oxygen (PaO2
) in the rat CPB model. Rats were divided into a SHAM group, a
hyperoxia CPB group (PaO2  > 400 mm Hg), and a normoxia CPB group
(PaO2 : 100-150 mm Hg). We measured the serum cytokine levels of tumor
necrosis factor-α, interleukin (IL)-6, and IL-10, and biochemical
markers (lactate dehydrogenase, aspartate aminotransferase, and alanine
aminotransferase) before, 60, and 120 min after the initiation of CPB.
We also measured the wet-to-dry weight (W/D) ratio of the left lung and
performed dihydroethidium (DHE) stain reflecting superoxide generation
in the lung and liver tissues 120 min after the CPB initiation. In the
hyperoxia group, the pro-inflammatory cytokines and biochemical markers
significantly increased during the CPB compared with the SHAM, but such
increases were significantly suppressed in the normoxia group. However,
the increase in anti-inflammatory cytokines was more suppressed in the
hyperoxia group than in the normoxia group. The W/D ratio increased
significantly more in the hyperoxia group than in the normoxia group. In
addition, the DHE fluorescence predominantly increased in the hyperoxia
group compared with that in the normoxia group. These data suggest that
it is better to avoid too much oxygen insufflation for attenuating
organ damage associated with the superoxide production and inflammatory
responses during CPB.